PREVALENCE OF MOLECULAR MARKERS OF PLASMODIUM FALCIPARUM RESISTANCE TO SULPHADOXINE/PYRIMETHAMINE IN CHILDREN WITH SICKLE CELL ANAEMIA AGED 6 TO 59 MONTHS IN BENIN CITY

Abstract

Intermittent Preventive Treatment (IPT) using sulphadoxine/pyrimethamine (SP) is a recent
chemoprevention method that has been shown to be efficacious in protecting infants and
young children including those with sickle cell anaemia (SCA) against malaria induced
morbidity and mortality. Unlike chemoprophylaxis, IPT using SP (IPT-SP) is affordable and
has a good delivery system and promotes drug compliance. However, one of the criteria for
the use of SP in IPT is the level of drug resistance in a region, as this has implications for the
efficacy of IPT-SP. Thus, evaluating and monitoring the level of P.falciparum resistance to
SP in a region prior to and during the use of IPT-SP is paramount. The use of molecular
markers of resistance is the most preferred method in evaluating and monitoring SP drug
resistance.
This was a cross-sectional comparative study assessing and determining the prevalence of
molecular markers of P.falciparum resistance to SP in children with SCA and their age and
sex matched control. In this study, 164 children with SCA aged 6-59 months with positive
blood smear for P.falciparum were recruited as subjects; and 164 children with HbAA with
positive blood smear for P.falciparum were recruited as controls.
The prevalence of molecular markers of P.falciparum resistance to SP in this study was high.
All subjects and control had molecular markers of resistance. The pfdhps A437G mutation
was 100% in children with HbAA and 97% in children with SCA, the pfdhfr triple mutant
genotype was 100% in children with SCA and 96% in children with HbAA. The presence of
A581G and A613S pfdhps mutations was reported in this study. The prevalence of
pfdhfr/pfdhps point mutations and that of pfdhps mutant genotype AGKGS were statistically
significantly higher in children with HbAA compared to those with SCA. The K540E and the
quintuple mutant genotype, which confer significant resistance to SP leading to treatment
failure, were totally absent in this study.